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myocardial metabolism

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26

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1

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1

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7

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2

Isotope-Labeled Compounds

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-158426
    2-APQC
    1 Publications Verification

    		 Sirtuin Cardiovascular Disease
    2-APQC is an orally active and selective agonist of Sirtuin-3 (SIRT3) (Kd=2.756 μM), antagonizes Isoproterenol/ISO (HY-B0468)-induced cytotoxicity. 2-APQC activates the SIRT3-PYCR1 axis to enhance mitochondrial proline metabolism and inhibit the ROS-p38MAPK pathway by inhibiting signaling pathways such as mTOR-p70S6K, JNK, and TGF-β/Smad3. 2-APQC also activates the AMPK-Parkin axis to alleviate myocardial hypertrophy and fibrosis and protect cardiac function. 2-APQC can be used in the study of heart failure .
    2-APQC
  • HY-N0806
    Sweroside
    3 Publications Verification

    		 Keap1-Nrf2 AMPK Sirtuin NF-κB NOD-like Receptor (NLR) Pyroptosis Apoptosis Autophagy PARP Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
    Sweroside is an iridoid glycoside that targets multiple targets, including the Keap1/Nrf2 axis, NLRP3 inflammasome, SIRT1, NF-κB, AMPK/mTOR pathway, and caspase family. Sweroside promotes Nrf2 nuclear translocation by competitively binding to Keap1. Sweroside also inhibits oxidative stress and NLRP3-mediated pyroptosis by activating Nrf2, inhibits NF-κB inflammatory pathway by activating SIRT1, and promotes autophagy and induces caspase-dependent apoptosis via the AMPK/mTOR pathway. Sweroside has antioxidant, anti-inflammatory, anti-apoptotic, and lipid metabolism regulating activities, and can be used in the research of myocardial ischemia-reperfusion injury, leukemia, acute lung injury, non-alcoholic fatty liver disease, and other fields .
    Sweroside
  • HY-121705
    Propionyl-L-carnitine

    		Endogenous Metabolite Apoptosis Bcl-2 Family NF-κB Survivin Src Akt AMPK NO Synthase Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Propionyl-L-carnitine is an orally active L-carnitine derivative. Propionyl-L-carnitine has a high affinity for muscle L-carnitine transferase. Propionyl-L-carnitine increases Apoptosis, Bax, and reduces NF-κB, VCAM-1, MCP-1, and survivin. Propionyl-L-carnitine activates Src kinase, Akt, induces p-AMPK and nitric oxide synthesis. Propionyl-L-carnitine alleviates cardiovascular disease, obesity, and colitis .
    Propionyl-L-carnitine
  • HY-N0712
    Typhaneoside
    3 Publications Verification

    		 mTOR Akt FXR PI3K Autophagy Ferroptosis Apoptosis Reactive Oxygen Species (ROS) Calcium Channel Cardiovascular Disease Neurological Disease Metabolic Disease Cancer
    Typhaneoside is an orally active activator of PI3K/Akt/mTOR and farnesoid X receptor. Typhaneoside promotes the activation of AMPK and Caspase-3, induces apoptosis, ferroptosis, autophagy, ROS accumulation, cell cycle arrest at the G2/M phase, and reduces cancer cell viability. Typhaneoside improves glucose and lipid metabolism, alleviates inflammatory responses, oxidative stress and hepatic lipid accumulation, and exerts hepatoprotective effects. Typhaneoside can be used in research related to heart failure after myocardial infarction, acute myeloid leukemia, non-alcoholic fatty liver disease and neurological disorders .
    Typhaneoside
  • HY-18282
    AZ876

    		LXR Cardiovascular Disease Metabolic Disease Cancer
    AZ876 is a selective, orally active agonist of liver X receptor (LXRα/β) (Ki=0.007 μM [LXRα, human], 0.011 μM [LXRβ, human]. AZ876 induces the expression of target genes such as ABCA1 and ABCG1, promotes reverse cholesterol transport (RCT) and regulates lipid metabolism and anti-inflammatory effects. AZ876 increases cardiac polyunsaturated fatty acid levels, reduces myocardial fibrosis, and reduces lesion area and monocyte adhesion in atherosclerosis models. AZ876 can be used in cardiovascular disease research, such as preventing and treating β-adrenergic-induced cardiac diastolic dysfunction and inhibiting the progression of atherosclerosis .
    AZ876
  • HY-P3016A
    Aspartate aminotransferase, porcine heart

    EC 2.6.1.1, porcine heart; GOT, porcine heart; AST, porcine heart

    		 Aminotransferases (Transaminases) Cardiovascular Disease
    Aspartate aminotransferase (EC 2.6.1.1), porcine heart is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, porcine heart comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, porcine heart also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, porcine heart is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers .
    Aspartate aminotransferase, porcine heart
  • HY-W016409
    Ethyl 3,4-dihydroxybenzoate
    1 Publications Verification

    Protocatechuic acid ethyl ester

    		 HIF/HIF Prolyl-Hydroxylase Reactive Oxygen Species (ROS) NO Synthase Autophagy Apoptosis Metabolic Disease Cancer
    Ethyl 3,4-dihydroxybenzoate (Protocatechuic acid ethyl ester) is an orally effective, blood-brain barrier-permeable, competitive prolyl hydroxylase (PHD) inhibitor that inhibits the hydroxylation modification of hypoxia-inducible factor (HIF) by PHD. Ethyl 3,4-dihydroxybenzoate stabilizes HIF-1α by inhibiting PHD, activates downstream pathways to induce autophagy and apoptosis of tumor cells, and regulates inflammatory responses, inhibits the NF-κB pathway, improves vascular permeability, and promotes osteoblast differentiation. Ethyl 3,4-dihydroxybenzoate has anti-tumor, anti-hypoxic injury, and bone metabolism regulation effects. It can also be used in the research of cardiovascular protection (such as reducing myocardial ischemic damage), bone tissue engineering (promoting osteogenesis/inhibiting osteoclast differentiation), and prevention and treatment of high-altitude cerebral edema .
    Ethyl 3,4-dihydroxybenzoate
  • HY-N0430
    Coptisine

    Coptisin

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine
  • HY-N0430A
    Coptisine Sulfate
    5 Publications Verification

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine Sulfate
  • HY-W011082
    NLRP3-IN-2

    		NOD-like Receptor (NLR) Cardiovascular Disease
    NLRP3-IN-2, an intermediate substrate in the synthesis of glyburide, inhibits the formation of the NLRP3 inflammasome in cardiomyocytes and limits the infarct size following myocardial ischemia/reperfusion in the mouse, without affecting glucose metabolism .
    NLRP3-IN-2
  • HY-139577
    Ninerafaxstat

    IMB-1018972; IMB-101

    		 Mitochondrial Metabolism Cardiovascular Disease Metabolic Disease
    Ninerafaxstat (IMB-1018972) is a novel orally active cardiac mitochondrial drug that restores myocardial energy homeostasis. Ninerafaxstat competitively inhibits 3-ketoacyl-CoA thiolase (3-KAT) to partially suppress fatty acid oxidation, and shifts cardiac energy metabolism from free fatty acid oxidation to glucose oxidation, regulating myocardial substrate utilization and thereby improving cardiac efficiency. Ninerafaxstat can be used for research on cardiovascular diseases .
    Ninerafaxstat
  • HY-P2799A
    Creatine Kinase (CPK/CK), Bovine Heart
    1 Publications Verification

    CK, CPK, Creatine Phosphokinase

    		 Endogenous Metabolite Creatine Kinase Cardiovascular Disease
    Creatine Kinase (CPK/CK), Bovine Heart (CK) is a creatine kinase derived from bovine heart. Creatine Kinase (CPK/CK), Bovine Heart catalyzes the reversible phosphate transfer reaction between phosphocreatine and ADP, and is widely used in myocardial energy metabolism research and quality control of clinical biochemical tests .
    Creatine Kinase (CPK/CK), Bovine Heart
  • HY-Y1322
    Triphenyl phosphate

    		Environmental Pollutants Mitophagy Apoptosis NF-κB p38 MAPK ERK JNK PI3K Akt Monoamine Oxidase Reactive Oxygen Species (ROS) PPAR Indoleamine 2,3-Dioxygenase (IDO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring .
    Triphenyl phosphate
  • HY-P3016
    Aspartate aminotransferase, Genetically engineered bacteria

    EC 2.6.1.1; GOT; AST

    		 Aminotransferases (Transaminases) Cardiovascular Disease
    Aspartate aminotransferase (EC 2.6.1.1), Genetically engineered bacteria is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, Genetically engineered bacteria comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, Genetically engineered bacteria also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, Genetically engineered bacteria is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers .
    Aspartate aminotransferase, Genetically engineered bacteria
  • HY-139577A
    Ninerafaxstat trihydrochloride

    MB-1018972 trihydrochloride; IMB-101 trihydrochloride

    		 Mitochondrial Metabolism Cardiovascular Disease Metabolic Disease
    Ninerafaxstat trihydrochloride (IMB-1018972 trihydrochloride) is the trihydrochloride salt form of Ninerafaxstat (HY-139577). Ninerafaxstat trihydrochloride is a novel orally active cardiac mitochondrial drug that restores myocardial energy homeostasis. Ninerafaxstat trihydrochloride competitively inhibits 3-ketoacyl-CoA thiolase (3-KAT) to partially suppress fatty acid oxidation, and shifts cardiac energy metabolism from free fatty acid oxidation to glucose oxidation, regulating myocardial substrate utilization and thereby improving cardiac efficiency. Ninerafaxstat trihydrochloride can be used for research on cardiovascular diseases .
    Ninerafaxstat trihydrochloride
  • HY-Y1322S
    Triphenyl phosphate-d15

    Celluflex TPP-d15; DHPF 005-d15; Disflamol TP-d15; Disflamoll TP-d15; NSC 57868-d15; Phenyl phosphate ((PhO)3PO)-d15; Phoscon FR 903N-d15

    		 Isotope-Labeled Compounds Environmental Pollutants ERK Indoleamine 2,3-Dioxygenase (IDO) p38 MAPK NF-κB Akt Monoamine Oxidase Mitophagy Reactive Oxygen Species (ROS) JNK PI3K PPAR Apoptosis Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Triphenyl phosphate-d15 is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.
    Triphenyl phosphate-d15
  • HY-P3016B
    Aspartate aminotransferase, Human liver

    EC 2.6.1.1, Human liver; GOT, Human liver; AST, Human liver

    		 Aminotransferases (Transaminases) Cardiovascular Disease
    Aspartate aminotransferase (EC 2.6.1.1), Human liver is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, Human liver comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, Human liver also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, Human liver is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers .
    Aspartate aminotransferase, Human liver
  • HY-18282R
    AZ876 (Standard)

    		LXR Cardiovascular Disease Metabolic Disease Cancer
    AZ876 (Standard) is the analytical standard of AZ876. This product is intended for research and analytical applications. AZ876 is a selective, orally active agonist of liver X receptor (LXRα/β) (Ki=0.007 μM [LXRα, human], 0.011 μM [LXRβ, human]. AZ876 induces the expression of target genes such as ABCA1 and ABCG1, promotes reverse cholesterol transport (RCT) and regulates lipid metabolism and anti-inflammatory effects. AZ876 increases cardiac polyunsaturated fatty acid levels, reduces myocardial fibrosis, and reduces lesion area and monocyte adhesion in atherosclerosis models. AZ876 can be used in cardiovascular disease research, such as preventing and treating β-adrenergic-induced cardiac diastolic dysfunction and inhibiting the progression of atherosclerosis .
    AZ876 (Standard)
  • HY-P2916
    Thymidine phosphorylase

    		Phosphorylase Cardiovascular Disease Neurological Disease Cancer
    Thymidine phosphorylase is a nucleoside metabolism enzyme that plays an important role in the pyrimidine salvage pathway. Thymidine phosphorylase catalyzes the conversion of thymidine to thymine and 2-deoxy-α-D-ribose-1-phosphate (dRib-1-P). Thymidine phosphorylase plays an important role in platelet activation in vitro and thrombosis in vivo by participating in multiple signaling pathways. Thymidine phosphorylase can be used for the study of myocardial infarction, stroke, pulmonary embolism and cancer .
    Thymidine phosphorylase
  • HY-101390B
    Niguldipine

    		Calcium Channel Cardiovascular Disease
    Niguldipine is a calcium channel blocker with activity in regulating cardiovascular function. Niguldipine can reduce systolic and diastolic blood pressure, thereby increasing heart rate and cardiac output. Niguldipine exhibits dose-dependent and sustained increases in coronary blood flow. Niguldipine also increases perfusion in the kidneys and femoral arteries, but the effect is temporary and to a lesser extent. The effect of Niguldipine on myocardial metabolism is not significant .
    Niguldipine
  • HY-W011082R
    NLRP3-IN-2 (Standard)

    		Reference Standards NOD-like Receptor (NLR) Cardiovascular Disease
    NLRP3-IN-2 (Standard) is the analytical standard of NLRP3-IN-2. This product is intended for research and analytical applications. NLRP3-IN-2, an intermediate substrate in the synthesis of glyburide, inhibits the formation of the NLRP3 inflammasome in cardiomyocytes and limits the infarct size following myocardial ischemia/reperfusion in the mouse, without affecting glucose metabolism .
    NLRP3-IN-2 (Standard)
  • HY-121586
    Nafazatrom

    Bay g 6575

    		 Lipoxygenase Cardiovascular Disease
    Nafazatrom (Bay g 6575) is an orally active cardioprotective agent that protects against ischemic damage. Nafazatrom dose-dependently inhibits neutrophil aggregation, superoxide anion generation, arachidonic acid metabolism, and to a lesser extent the release of β-glucosidase, platelet aggregation or arachidonic acid in vitro. Acid metabolism has no significant effect. In a dog ischemia-reperfusion model, Nafazatrom (10 mg/kg; po) reduced infarct size and the occurrence of arrhythmias and rescued ischemic myocardial function without affecting any hemodynamic changes. The basis of Nafazatrom's cardioprotection may be inhibition of neutrophil function and cellular infiltration in vitro .
    Nafazatrom
  • HY-N0806R
    Sweroside (Standard)

    		Reference Standards Keap1-Nrf2 AMPK Sirtuin NF-κB NOD-like Receptor (NLR) Pyroptosis Apoptosis Autophagy PARP Metabolic Disease
    Sweroside (Standard) is the analytical standard of Sweroside (HY-N0806). This product is intended for research and analytical applications. Sweroside is an iridoid glycoside that targets multiple targets, including the Keap1/Nrf2 axis, NLRP3 inflammasome, SIRT1, NF-κB, AMPK/mTOR pathway, and caspase family. Sweroside promotes Nrf2 nuclear translocation by competitively binding to Keap1. Sweroside also inhibits oxidative stress and NLRP3-mediated pyroptosis by activating Nrf2, inhibits NF-κB inflammatory pathway by activating SIRT1, and promotes autophagy and induces caspase-dependent apoptosis via the AMPK/mTOR pathway. Sweroside has antioxidant, anti-inflammatory, anti-apoptotic, and lipid metabolism regulating activities, and can be used in the research of myocardial ischemia-reperfusion injury, leukemia, acute lung injury, non-alcoholic fatty liver disease, and other fields .
    Sweroside (Standard)
  • HY-W778057
    Ethyl 3,4-Dihydroxybenzoate-13C3

    Protocatechuic acid ethyl ester-13C3

    		 Reactive Oxygen Species (ROS) Cancer
    Ethyl 3,4-Dihydroxybenzoate- 13C3 (Protocatechuic acid ethyl ester- 13C3) is the 13C-labeled Ethyl 3,4-dihydroxybenzoate (HY-W016409). Ethyl 3,4-dihydroxybenzoate (Protocatechuic acid ethyl ester) is an orally effective, blood-brain barrier-permeable, competitive prolyl hydroxylase (PHD) inhibitor that inhibits the hydroxylation modification of hypoxia-inducible factor (HIF) by PHD. Ethyl 3,4-dihydroxybenzoate stabilizes HIF-1α by inhibiting PHD, activates downstream pathways to induce autophagy and apoptosis of tumor cells, and regulates inflammatory responses, inhibits the NF-κB pathway, improves vascular permeability, and promotes osteoblast differentiation. Ethyl 3,4-dihydroxybenzoate has anti-tumor, anti-hypoxic injury, and bone metabolism regulation effects. It can also be used in the research of cardiovascular protection (such as reducing myocardial ischemic damage), bone tissue engineering (promoting osteogenesis/inhibiting osteoclast differentiation), and prevention and treatment of high-altitude cerebral edema .
    Ethyl 3,4-Dihydroxybenzoate-13C3
  • HY-W016409R
    Ethyl 3,4-dihydroxybenzoate (Standard)

    Protocatechuic acid ethyl ester (Standard)

    		 Reference Standards HIF/HIF Prolyl-Hydroxylase Reactive Oxygen Species (ROS) NO Synthase Autophagy Apoptosis Metabolic Disease Cancer
    Ethyl 3,4-dihydroxybenzoate (Standard) (Protocatechuic acid ethyl ester (Standard)) is the analytical standard of Ethyl 3,4-dihydroxybenzoate (HY-W016409). This product is intended for research and analytical applications. Ethyl 3,4-dihydroxybenzoate (Protocatechuic acid ethyl ester) is an orally effective, blood-brain barrier-permeable, competitive prolyl hydroxylase (PHD) inhibitor that inhibits the hydroxylation modification of hypoxia-inducible factor (HIF) by PHD. Ethyl 3,4-dihydroxybenzoate stabilizes HIF-1α by inhibiting PHD, activates downstream pathways to induce autophagy and apoptosis of tumor cells, and regulates inflammatory responses, inhibits the NF-κB pathway, improves vascular permeability, and promotes osteoblast differentiation. Ethyl 3,4-dihydroxybenzoate has anti-tumor, anti-hypoxic injury, and bone metabolism regulation effects. It can also be used in the research of cardiovascular protection (such as reducing myocardial ischemic damage), bone tissue engineering (promoting osteogenesis/inhibiting osteoclast differentiation), and prevention and treatment of high-altitude cerebral edema .
    Ethyl 3,4-dihydroxybenzoate (Standard)
  • HY-P3016C
    Aspartate aminotransferase, Human (HEK293)

    EC 2.6.1.1, Human (HEK293); GOT, Human (HEK293); AST, Human (HEK293)

    		 Aminotransferases (Transaminases) Cardiovascular Disease
    Aspartate aminotransferase (EC 2.6.1.1), Human (HEK293) is a metabolic regulator with the highest activity in the heart, liver and skeletal muscle. Aspartate aminotransferase, Human (HEK293) comprises two isozymes: the cytoplasmic form (AST1) and the mitochondrial form (AST2). By catalyzing reversible transamination reactions between oxaloacetate, L-glutamate and other substances, it is deeply involved in key physiological processes such as amino acid metabolism, the tricarboxylic acid cycle and neurotransmitter synthesis. Aspartate aminotransferase, Human (HEK293) also provides substrate support for the synthesis of urea and purines/pyrimidines. Aspartate aminotransferase, Human (HEK293) is a serum marker reflecting cardiac and hepatic injury, and its abnormal levels are also closely associated with myocardial infarction, cardiovascular diseases and various cancers .
    Aspartate aminotransferase, Human (HEK293)

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